There is increasing appreciation for the role of the endothelium in orchestrating the host response to infection and injury, as occurs in sepsis, trauma, or surgery. An urgent need exists to identify novel therapies that attenuate or modify the host response and thus improve patient outcome. This chapter focuses on the nature and mechanisms of coagulopathy associated with trauma, particularly that related to combat injury. Trauma-related coagulopathy is qualitatively different from that seen in sepsis and surgery. Trauma suffered in combat, as distinct from civilian life, introduces additional variables that may impact on the bleeding phenotype. Although at present we have little understanding of how the endothelium is influenced by and/or mediates the host response in trauma, it seems likely that this organ will ultimately serve as an important diagnostic tool and therapeutic target.

NATURE OF COMBAT WOUNDS

Causes of Death

Approximately 50% of those who die from combat injury die from exsanguinating hemorrhage, which is the leading cause of death from combat trauma (1,2). Historically, a small percentage of these deaths have been from sites where the bleeding might be controlled by compression. This population of casualties will be reduced through the use of improved training for self care, medics, and other first-responder personnel, coupled with effective equipment like improved tourniquets or hemostatic dressings. The military has aggressively and successfully pursued these measures. The largest percentage of potentially preventable hemorrhagic combat deaths, however, is due to noncompressible (internal) hemorrhage (47%). The challenge is to develop means with which medics can initiate control of truncal hemorrhage through nonsurgical means. This represents a significant research hurdle.